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The functional immaturities of the cells responsible for the innate defense in neonates have often been considered a significant risk factor for perinatal infections. The ability of the neutrophils and monocytes to generate reactive oxygen species (ROS) is mandatory for efficient killing of bacteria and fungi. This study aimed to assess the production of reactive oxygen species (ROS), as well as the differences in leucocyte populations in healthy preterm and term neonates, using healthy adults as controls. Burst activation of peripheral blood phagocytes (PBPs) was quantified by using a flow cytometry method that implied incubation of peripheral whole blood phagocytes with various stimuli that included an opsonized Escherichia coli and a non-opsonized Candida albicans yeast suspension. We observed a smaller population of activated granulocytes after exposure to E. coli in premature neonates than in control adults (41.19±20.63% vs. 58.32±33.46%, p=0.058). Monocyte burst activation triggered by E. coli, although lower in preterm than in control adults was not significantly different (38.97±20.73% vs. 46.82±21.05%, p>0.05). Incubation with non-opsonized C. albicans led to a similar low granulocyte and monocyte activation in all studied groups, reaching a statistically significant difference only between term neonates and adults. The study shows a deficit of the premature neonate granulocyte to generate ROS when exposed to opsonized E.coli. The preterm and term, as well as the adult PBPs presented an almost similar low oxidative burst when exposed to C. albicans, in spite of evoked functional immaturity of the preterm neonate phagocytes.

Oxidative Burst of Neonatal and Adult Peripheral Blood Phagocytes Confronting Escherichia coli and Candida albicans